Speed and diffusion of kinesin-2 are competing limiting factors in flagellar length control model
Abstract
Flagellar length control in Chlamydomonas is a tractable model system for studying the general question of organelle size regulation. We have previously proposed that diffusive return of the kinesin motor that powers intraflagellar transport can play a key role in length regulation. Here we explore how the motor speed and diffusion coefficient for the return of kinesin-2 affect flagellar growth kinetics. We find that the system can exist in two distinct regimes, one dominated by motor speed and one by diffusion coefficient. Depending on length, a flagellum can switch between these regimes. Our results indicate that mutations can affect length in distinct ways. We discuss our theory’s implication for flagellar growth influenced by beating and provide possible explanations for the experimental observation that a beating flagellum is usually longer than its immotile mutant. These results demonstrate how our simple model can suggest explanations for mutant phenotypes.
Statement of Significance
The eukaryotic flagellum is an ideal case study in organelle size control because of its simple linear shape and well-understood building mechanism. In our previous work, we proved that flagellar length in the green algae Chlamydomonas can be controlled by the diffusive gradient of the kinesin-2 motors that deliver building blocks to the tip. In this study, we expand on the analytical formulation of the diffusion model to show how physical parameters affect final length and regeneration time, enhancing the model’s potential to explain length mutants and motivate future research with precise predictions.
